War Surgery

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WARSURGERYWORKING WITH LIMITED RESOURCES

IN ARMED CONFLICT

AND OTHER SITUATIONS OF VIOLENCE

VOLUME 2

C. GiannouM. BaldanÅ. Molde


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International Committee of the Red Cross

19, avenue de la Paix

1202 Geneva, Switzerland

T +41 22 734 60 01 F +41 22 733 20 57

E-mail: [email protected] www.icrc.org

© ICRC, March 2013

Cover photos: M. Baldan / ICRC; Michael Zumstein / Agence VU’; E. Erichsen / Aira Hospital, Ethiopia


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WARSURGERYWORKING WITH LIMITED RESOURCES

IN ARMED CONFLICT

AND OTHER SITUATIONS OF VIOLENCE

VOLUME 2

C. GiannouM. BaldanÅ. Molde


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PREFACE

It is with great pleasure that I welcome the completion of Volume 2 of War Surgery: Working withLimited Resources in Armed Conflict and Other Situations of Violence. As did Volume 1, this second

volume has benefited from numerous remarkable professional collaborations and scientificcontributions under the joint authorship and review of Drs Christos Giannou, Marco Baldanand Åsa Molde. I feel certain that it will provide a new point of reference for health professionalsengaged in providing lifesaving services in often hazardous environments.

Most fortuitously, the publication of Volume 2 coincides with the 150th anniversary of thefounding of the International Committee of the Red Cross. The historical importance of thisanniversary for professionals engaged in war surgery cannot be overstated. In 1863, a groupof Swiss citizens created the International Committee of Geneva for the Relief of WoundedSoldiers, which heralded the dawn of a new consciousness regarding the fate of thewounded left incapacitated on the battlefield. The history of the ICRC and the Red Cross/RedCrescent Movement is intimately interwoven with the development of war surgery, both as aprofessional discipline and as an ethos in times of armed conflict.

The ICRC’s future will be shaped by its commitment to continuous learning and to theenhancement of the professionalism of humanitarian action. This new manual bears testimonyto the dedication of Red Cross and Red Crescent surgeons in articulating and sharing theirexperiences to prepare a new generation of professionals equipped and empowered to bethe future standard-bearers for war surgery.

Since the publication of Surgery for the Victims of War in 1985, the ICRC has accomplished a greatdeal – although much remains to be done – in defining the appropriate treatment protocols forthe management of the war wounded when working in resource-poor settings: a continuousexercise of updating and expanding relevant and appropriate knowledge to help save lives

and alleviate suffering in spite of the prevailing and often dire conditions.

Consequently, this manual is first and foremost accountable to the people and communitiesit seeks to serve. In addition, in the pursuit of protecting and assisting the victims of armedconflict and other situations of violence, the ICRC insists on the safeguarding of medicalneutrality and accessibility of medical care to those in need as a fundamental message ofthe International Movement of the Red Cross and Red Crescent and of all humanitarian work.Indeed, to use the words of the Health Care in Danger campaign: “It’s a matter of life and death”.

Peter Maurer

PresidentInternational Committee of the Red Cross


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Chapter 21 INJURIES DUE TO ANTIPERSONNEL MINES 5121.1 Introduction: the humanitarian challenge 5321.2 Mechanism of injury 5421.3 Clinico-pathological patterns of injury 5521.4 Epidemiology 5721.5 Blast mine injury: pathogenesis and clinical implications 6021.6 Clinical presentation and management 6421.7 Surgical management of pattern 1 traumatic amputations 66

21.8 Special features of mine-blast injury to the foot 6821.9 Special features of mine-blast injury to the hand: pattern 3 6921.10 Surgical management of pattern 2 injuries 6921.11 Physical and psychological rehabilitation 7021.12 Conclusion: the humanitarian challenge 70Annex 21. A Humanitarian repercussions of landmines 71

Part B LIMBS 75

B.1 Introduction 77B.2 Wound ballistics 78B.3 Epidemiology 78

B.4 Emergency room care 80B.5 Surgical decision-making 82B.6 Patient preparation 85B.7 Surgical treatment 86B.8 Topical negative pressure and vacuum dressing 90B.9 Crush injury of the limbs: rhabdomyolysis 90B.10 Compartment syndrome and fasciotomy 91B.11 Reconstructive surgery of the limbs 96Annex B.1 Pneumatic tourniquet 97Annex B.2 Crush injury 98

Chapter 22 INJURIES TO BONES AND JOINTS 10322.1 Introduction 10522.2 Wound ballistics 10522.3 Epidemiology 10922.4 Management of war wounds with fractures 11222.5 Methods of bone immobilization: surgical decision-making 11422.6 Wounds involving joints 12122.7 Hand and foot injuries 12322.8 Problematic cases 12522.9 Bone infection 12722.10 Bone grafting 131Annex 22. A Plaster-of-Paris 133

Annex 22. B Traction 145Annex 22. C External fixation 156Annex 22. D ICRC chronic osteomyelitis study 163Annex 22. E Bone grafting 166

Chapter 23 AMPUTATIONS AND DISARTICULATIONS 17123.1 Introduction 17323.2 Epidemiology 17423.3 Surgical decision-making 17523.4 Classical surgical procedure: initial operation 17723.5 Delayed primary closure 18023.6 Myoplastic amputations 18123.7 Guillotine amputation 18823.8 Specific amputations and disarticulations 18923.9 Post-operative care 19523.10 Patient rehabilitation 19523.11 Complications and stump revision 197


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Chapter 24 VASCULAR INJURIES 20124.1 Introduction 20324.2 Wound ballistics and types of arterial injury 20324.3 Epidemiology 20524.4 Emergency room care 20824.5 Diagnosis and surgical decision-making 20924.6 Surgical management 21024.7 Post-operative care 217

24.8 Damage control and temporary shunt 21724.9 Complex limb injuries: concomitant arterial lesion and fracture 21924.10 Specific arteries 21924.11 Venous injury 22024.12 Arterio-venous fistula and pseudoaneurysm 22124.13 Complications 223

Chapter 25 INJURY TO PERIPHERAL NERVES 22525.1 Introduction 22725.2 Wound ballistics 22725.3 Pathophysiology 227

25.4 Epidemiology 22825.5 Clinical picture 22925.6 Surgical management 23025.7 Surgical technique of nerve suture 23325.8 Post-operative care 23525.9 Post-trauma sequelae 236

Part C HEAD, FACE, AND NECK 239

C.1 The general surgeon and the head, face and neck 242

Chapter 26 CRANIOCEREBRAL INJURIES 24526.1 Introduction 24726.2 Mechanisms of injury and wound ballistics 24826.3 Epidemiology 25026.4 Pathophysiology 25326.5 Clinical examination 25426.6 Emergency room management 25626.7 Decision to operate 25726.8 Operating theatre 25826.9 Cranio-cerebral debridement: “burr-hole” wound 26026.10 Tangential wounds 26326.11 Other penetrating wounds 26626.12 Trepanation 268

26.13 Difficult situations 26826.14 Post-operative and conservative management 27226.15 Increased intracranial pressure 27426.16 Cerebrospinal fluid fistula 27526.17 Infection 27526.18 Primary blast neurotrauma 27626.19 Post-trauma rehabilitation 277Annex 26. A Trepanation 278


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Chapter 27 MAXILLOFACIAL INJURIES 28327.1 Introduction 28527.2 Wound ballistics 28627.3 Epidemiology 28727.4 Clinical examination and emergency room care 28827.5 Decision to operate 29027.6 Haemostasis and debridement 29227.7 Mandibular fractures 295

27.8 Midface fractures 30127.9 Skin closure 30427.10 Post-operative management 30527.11 Complications 306

Chapter 28 INJURIES TO THE EAR 30928.1 Epidemiology and mechanism of wounding 31128.2 External ear 31128.3 Middle ear 31228.4 Inner ear 313

Chapter 29 INJURIES TO THE EYE 31529.1 Introduction 31729.2 Wounding mechanisms and ballistics 31829.3 Epidemiology 31929.4 First aid and emergency care 32029.5 Clinical picture and examination 32029.6 Primary management 32329.7 Assessment of injury and decision to operate 32329.8 Anaesthesia 32429.9 Minor procedures 32529.10 Intermediate injuries 32729.11 Excision of the eye 32929.12 Retrobulbar haemorrhage 33129.13 Treatment of complications 33229.14 Burns of the eyelids and eye 333Annex 29. A Complete ocular examination 334

Chapter 30 INJURIES TO THE NECK 33730.1 Introduction 33930.2 Surgical anatomy 33930.3 Wound ballistics 34130.4 Epidemiology 34130.5 Clinical presentations and emergency room care 343

30.6 Decision to operate 34730.7 Patient preparation 34730.8 Surgical management of vascular injuries 34830.9 Surgical management of laryngo-tracheal injuries 35230.10 Surgical management of pharyngo-oesophageal injuries 35430.11 Post-operative care 35530.12 Tracheostomy 356

Part D TORSO 359

D.1 Introduction 361D.2 Epidemiology 361D.3 Thoraco-abdominal wounds 362D.4 Injuries to the diaphragm 364D.5 Transaxial injuries 365D.6 Junctional trauma 365D.7 The general surgeon and the chest: the psychological partition 366


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Chapter 31 THORACIC INJURIES 36931.1 Introduction 37131.2 Wound ballistics 37131.3 Epidemiology 37331.4 Clinical presentation 37631.5 Emergency room management 38031.6 Intercostal chest tube drainage 38131.7 Thoracotomy 385

31.8 Exploration of the chest cavity 39031.9 Wounds of the chest wall 39131.10 Injuries of the lung 39131.11 Great vessels, heart and pericardium 39531.12 Oesophageal injuries 39831.13 Other injuries 39931.14 Thoracic damage control 40031.15 Post-operative care after thoracotomy 40031.16 Retained haemothorax 40131.17 Empyema 402Annex 31. A Intercostal nerve block 405

Annex 31. B Intercostal chest tube 406Annex 31. C Thoracic incisions 412

Chapter 32 INJURIES TO THE ABDOMEN 41932.1 Introduction 42132.2 Wound ballistics 42132.3 Epidemiology 42532.4 Clinical presentations 43232.5 Emergency room management 43432.6 Decision to operate 43632.7 Preparation of the patient and anaesthesia 43732.8 General plan of surgery 43832.9 Damage control: abbreviated laparotomy 44232.10 “Frontline laparotomy” and late-presenting patients 44532.11 Midline great vessels 44632.12 Liver and biliary tract 45032.13 Pancreas, duodenum and spleen 45832.14 Stomach 46532.15 Small bowel 46632.16 Colon 46832.17 Pelvis 47432.18 Abdominal drains 47832.19 Post-operative care 479

32.20 Post-operative complications 480Annex 32. A Abdominal compartment syndrome 482

Chapter 33 UROGENITAL TRACT INJURIES 48533.1 Introduction 48733.2 Wound ballistics 48733.3 Epidemiology 48733.4 Examination and diagnosis 48833.5 Kidneys 48833.6 Ureters 49433.7 Urinary bladder 50033.8 Prostate and posterior urethra 50133.9 Male external genitalia and anterior urethra 50333.10 Female genitalia and urethra 50633.11 Post-operative care 507


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Chapter 34 AUTOTRANSFUSION 50934.1 Rationale of autotransfusion 51134.2 Methodology of autotransfusion 51234.3 Pathophysiological changes 51334.4 Indications 51434.5 Practical autotransfusion methods 51534.6 Complications and risks 519

Chapter 35 WAR WOUNDS IN PREGNANT WOMEN 52335.1 Introduction 52535.2 Wound ballistics 52535.3 Epidemiology and international humanitarian law 52535.4 Clinical picture and emergency room care of the mother 52735.5 Examination of the foetus 52935.6 Surgical decision-making 53035.7 Surgery of the abdomen 53135.8 Post-operative care 532

Part E SPINE 535

Chapter 36 INJURIES OF THE VERTEBRAL COLUMN AND SPINAL CORD 54136.1 Wound ballistics 54336.2 Epidemiology 54436.3 Pathophysiology 54536.4 Clinical picture and examination 54636.5 Emergency room management 55036.6 Surgical decision-making 55236.7 Organization of further management 55336.8 Skin care 55436.9 Care of the bladder 55536.10 Nutrition and care of the bowels 55836.11 Physiotherapy and mobilization 55836.12 Complications 560Annex 36. A Hospital nursing care 563

Part F HOSPITAL MANAGEMENT AND PATIENT CARE 571

F.1 Hospital management 573F.2 Post-operative care 574F.3 Critical care in low-income countries 578F.4 Improvisation 580F.5 Final remarks 582Annex F. 1 Ballistics 583

Annex F. 2 Red Cross Wound Score and classification system 586Annex F. 3 ICRC antibiotic protocol 588

ACRONYMS 591

SELECTED BIBLIOGRAPHY 595


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INTRODUCTION TO VOLUME 2


Volume 1 of this manual has been well received by its target audience: surgeonsof the Red Cross/Red Crescent Movement and other humanitarian agencies, and

civilian and military colleagues working in austere, constrained and at times hostileenvironments. While Volume 1 dealt with general themes and topics, the challengeof Volume 2 lies in applying the same logic to the management of actual wounds inspecific organ systems.

Different socio-economic and tactical contexts call for different “surgeries” for thevictims of war as described in Sections 1.3 and 6.5 in Volume 1. No one model oforganization of surgical care can meet the demands and constraints of very differentcontexts. The context may be military or civilian and involve a wealthy industrializedsociety, an emerging economy, or a low-income country. The constraints are relatedto security; efficiency of pre-hospital care and patient evacuation; the supply ofmedicines and consumables and the repair and maintenance of equipment; and ofcourse the availability of human resources, both in terms of numbers and technicalcompetency. All too often, while facing a barrage of war casualties, hospital staff findthemselves working in conditions bereft of the resources necessary to provide optimalpatient care. It is under these circumstances that the application of appropriate clinicaltechniques and protocols employing appropriate technology come to the fore infulfilling their lifesaving potentials given the constraints – material and human.

Inevitably, the techniques described are not those of the latest developments asperformed by specialists working in an academic setting. Many are a throwbackto what was expected of a general surgeon one or two generations ago. That suchtechniques are still scientifically valid today is a tribute to our predecessors andthey still form the basis of good surgical practice in many countries where, even inpeacetime, resources are limited and working circumstances precarious.

As mentioned, this manual is geared to the needs of the trained general surgeonworking more or less in isolation in a rural hospital where referral of patients tomore sophisticated facilities – far away in an inaccessible major city – is impracticalor impossible. It also recognizes the great variety of technical competency andprofessional experience of its readers. This is why, for example, the operative details ofboth chest tube drainage and a thoracotomy are described.

The surgical management of the various organ systems of the body is subdivided intosurgical subspecialties, such as neurosurgery, maxillo-facial surgery, ophthalmologyand otorhinolaryngology, chest and vascular surgery, and orthopaedics. The general

surgeon will usually have only a passing knowledge of the procedures required todeal with trauma affecting these different organ systems. Nonetheless, a great dealcan be done by applying simple and basic techniques well within the competency ofthe general surgeon. The operations described are those that have proved successfulin the experience of ICRC surgeons and other colleagues working in similar conditions.


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More sophisticated procedures, particularly of reconstructive surgery, do indeedrequire the expertise of the specialist, and are not dealt with in this book.

We hope that well-trained specialist surgeons working in resource-poor settings willalso find this ICRC experience useful and relevant, since the constraints of limitedresources mean that the surgeon must accept that he cannot fully utilize his capacitiesand expertise, owing to a lack of diagnostic equipment and therapeutic means, suchas blood for transfusion.

Moreover, the limits of the surgery that can be performed are most often determinedby the level of anaesthesia, post-operative nursing care and physiotherapy available.In this respect too, the surgeon working in a resource-poor environment carries aparticular responsibility and must, for instance, be able and willing to personally makethe patient cough and breathe deeply and get the patient out of bed and walkingand exercising.

Volume 2 of this manual deals with trauma specific to armed conflict. Blunt injuriesalso occur during war, but will only be mentioned to indicate what distinguishes themfrom injuries caused by projectiles and blast.

The chapters fall into a similar pattern. They start with the particularities of ballistics

as applied to the organs of that region, and include a brief overview of the relevantepidemiology and the most important clinico-pathological presentations. Thesesections are followed by a description of the paraclinical investigations using theappropriate level of technology as is warranted by ICRC experience. Pre-operative andoperative procedures, according to ICRC protocols, are then explained. Basic patientmonitoring with limited means and post-operative care and physiotherapy completethe management sequence. The most common complications close the chapter.

As expressed in the Introduction to Volume 1, the authors hope that colleagues facingthe challenge of treating the victims of armed conflict and other situations of violenceunder precarious and, at times dangerous, circumstances will find this book useful.

Christos Giannou

Senior ICRC surgeon,former ICRC head surgeon

Marco Baldan

Senior ICRC surgeon,former ICRC head surgeon

Åsa Molde

Senior ICRC surgeon,former Coordinator ofICRC surgical programmes,and former Vice-PresidentSwedish Red Cross Society


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Please note:

Three annexes have been added to Part F to facilitate the reading of this Volume. Theyinclude a short summary of wound ballistics, the Red Cross Wound Score, and theICRC antibiotic protocols. Including them in Volume 2 allows for a quick reference. Fordetailed explanations, the reader should refer to the relevant chapters in Volume 1.

The manual, a film on the treatment of anti-personnel landmine injuries, and ICRCbrochures dealing with physiotherapy techniques, the application of plaster-of-Paris

and bone traction, and polypropylene technology for prostheses are included inthe DVD attached to this volume. The disk also contains several downloadable files

– annexes for the home care of spinal injury patients – written in simple English thatcan be translated and adapted for use in the everyday practice of home-care teams.

Cross references to topics presented in Volume 1 are given as references to a specificchapter or section without repeating the mention of Volume 1.

Many readers of this book are not native English speakers. Consequently both styleand vocabulary have been chosen with this readership in mind and certain well-known abbreviations have been spelt out. Unless stated otherwise masculine nounsand pronouns do not refer exclusively to men, for the manual is gender neutral. Any

use of trade or brand names is for illustrative purposes only and does not imply anyendorsement by the ICRC. No patient was photographed without consent – explicitor implicit.

This volume supersedes and replaces several ICRC publications that will no longerbe available. The knowledge and experience expressed in these works form thecontinuing basis of ICRC surgical protocols.

• Surgery for Victims of War , by Daniel Dufour, Soeren Kromann Jensen,Michael Owen-Smith, Jorma Salmela, G. Frank Stening, and Björn Zetterström.Second edition edited by Robin Gray; third edition revised and edited by Åsa Molde.

• Amputation for War Wounds, by Robin M. Coupland.

• War Wounds with Fractures: A Guide to Surgical Management , by David I. Rowley.

The authors have not received any outside remuneration for this manual and declareno conflict of interest.


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Acknowledgements

Volume 2 concludes the updating of Surgery for Victims of War , first published bythe ICRC in 1988. In addition, several chapters have made extensive use of the ICRCbrochures by Robin Coupland, Amputations for War Wounds (1992), and David I. Rowley,Professor of Orthopaedic and Trauma Surgery, University of Dundee, War Wounds withFractures: A Guide to Surgical Management (1996).

The authors of the present manual and all ICRC surgeons owe a debt of gratitude to

the pioneering work of their predecessors, and the clear and simple approach that hascontinued to serve as a model.

This Volume has benefited from the comments of many colleagues with muchexperience within and outside the ICRC. Valuable advice throughout was provided by:

Ken Barrand (UK)

Mauro Della Torre (Italy)

Herman Du Plessis (South Africa)

Jacques Goosen (South Africa)

Hans Husum (Norway)

Jorma Salmela (Finland)

Valery Sasin (Byelorussia)

Harald Veen (Netherlands)

Günter Wimhoefer (Germany).

Daniel Brechbuehler (Switzerland), Victor Uranga (Mexico), and Björn Zackari (Sweden)also contributed comments to various chapters.

Beat Kneubuehl (Switzerland) acted as the scientific adviser on ballistics and blasteffects. Ben Lark (UK) of the ICRC was solicited for technical advice on blast phenomena.The course on wound ballistics given by M.C. Jourdan at the Hôpital d’Instructiondes Armées, Ste Anne, Toulon, France, was kindly made available. Dominique Loye(Switzerland) of the ICRC served as technical adviser on matters pertaining to weaponsand international humanitarian law.

David Rowley (UK) and Richard Gosselin (Canada) served as technical advisers on

orthopaedics, as did Michel Richter (Switzerland) on maxillo-facial injuries andAlain Reverdin (Switzerland) for cranio-cerebral wounds. Fabrice Jamet (France) andHelena Iaasonen (Finland) were technical advisers on war wounds in pregnant womenand Assad Muhyddin Taha (Lebanon) on wounds of the torso. Michael Baumbergerand Karin Roth of the Swiss Paraplegic Centre in Nottwil provided useful commentson spinal cord injury and Mahiban Thomas (India – Australia) on maxillo-facial injuries.

Astute observations and quotable quotes were contributed by Tim Hardcastle(South Africa) and Louis Riddez (Sweden) and permission to quote was also extendedby Norman E. McSwain Jr (USA) and Jean-Louis Vincent (Belgium).

The Second ICRC Master Surgeons Workshop, held in Geneva in December 2010,revised the ICRC protocols on antibiotics, nutrition, and the management of chesttube drainage and skeletal traction amongst other topics. Participants included:

Joseph Adase (Ghana)

Marco Baldan (Italy)

Ken Barrand (UK)

Massey Beveridge (Canada)

Daniel Brechbuehler (Switzerland)

Amilcar Contreras (El Salvador)

Mauro Della Torre (Italy)

Jean-Marc Fiala (Switzerland)

Marco Garatti (Italy) representingthe non-governmental organizationEMERGENCY

Christos Giannou (Greece – Canada)

Richard Gosselin (Canada)

Fabrice Jamet (France)

Paul MacMaster (UK) representingMédecins Sans Frontières (MSF)Netherlands


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Tesfaye Makonnen (Ethiopia)

Alberto Nardini (Italy)

Hassan Nasreddine (Lebanon– Switzerland)

Valery Sasin (Byelorussia)

Enrique Steiger (Switzerland)

Kazmer Szabo (Hungary)

Harald Veen (Netherlands)

Julio Guibert Vidal (Peru)

Günter Wimhoefer (Germany).

The authors were pleased that collaborators for Volume 1 also participated in theproduction of this volume: Christiane de Charmant handled the editing of the finaltext and was responsible for the production while Lisa Zeitoun and Pierre Gudelof SimpleCom Graphics, Yverdon, Switzerland provided the graphic design. Theircontribution, as always, is greatly appreciated.

Permissions and assistance

Apart from ICRC surgeons, a number of colleagues have made photographs availablefor this manual. The authors wish to thank Takashi Shiroko and Masaharu Nakade ofthe Japanese Red Cross Society; Franco Plani at the Chris Hani Baragwanath Hospital,Soweto, South Africa; Gamini Goonetilleke, Sri Jayewardenapura General Hospital,and Past President of the College of Surgeons of Sri Lanka; K.N. Joshi, Lumbini Zonal

Hospital, Nepal; Dan Meckelbaum, McGill University Hospital; Rusta Saleah,Pattini Provincial Hospital, Thailand; Burapat Sangthong, Songkla University Hospital,Thailand; Michael Stein, Rabin Medical Center – Beilinson Hospital, Petach-Tikva,and Chairman of Israel Trauma Society; Assad Taha, American University of BeirutMedical Center; Moufid Yacoub, Rafidia Hospital, Nablus, West Bank (Palestine); andAssefa Weldu at the Army General Hospital, Addis Ababa, Ethiopia.

The authors also wish to thank the Surgical Centre for War Victims, EMERGENCY, Kabul,Afghanistan; and Erik Erichsen and the Aira Hospital, Oromia Region, Ethiopia, forpermission to use their photographs.

In addition, Figure A.5, Crown Copyright, was reproduced with the kind permission ofthe Editor of the Journal of the Royal Army Medical Corps. Permission was granted bythe authors of Bryusov PG, Shapovalov VM, Artemyev AA, Dulayev AK, Gololobov VG.Combat Injuries of Extremities. Moscow: Military Medical Academy, GEOTAR; 1996 andNechaev EA, Gritsanov AI, Fomin NF, Minnullin IP, eds. Mine Blast Trauma: Experiencefrom the War in Afghanistan. St Petersburg: Russian Ministry of Public Health andMedical Industry, Vreden Research Institute of Traumatology; 1995, to use and adaptsome of their drawings.

The authors must mention Maurice King, editor, Primary Surgery , as the inspirationfor a number of drawings that have been adapted by the ICRC artist. This book wasfirst published by Oxford University Press and is now available at http://www.primary-surgery.org/ps/vol2/html/index.html through the generosity of GTZ, the GermanAgency for Technical Cooperation. Reproduction of the originals was not possiblefor technical reasons. The ICRC artist was Nikos Papas, whose collaboration wasmost welcome.

The Editor of Military Medicine: International Journal of AMSUS (Association of MilitarySurgeons of the United States) assisted in the research by making certain articlesavailable. In addition, the senior author is greatly indebted to the Ptolemy Projectof the Office of International Surgery, University of Toronto, Canada, which providedinternet access to the university library. This access was indispensable for the researchnecessary in the writing of both Volumes 1 and 2 of this manual.


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Part A

BLAST PHENOMENA


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A BLAST PHENOMENA

A.1 Short history of the weapons of war and armed conflict 19

A.2 Munition composition 20

A.3 Open-air bomb explosion 20A.3.1 Positive-pressure shock wave 21A.3.2 Negative-pressure suction wave 21

A.3.3 Blast wind 21A.4 Effects due to the environment 21

A.5 Specific explosive devices 22A.5.1 Enhanced-blast explosive devices 22A.5.2 Shaped-charge explosives 22A.5.3 Improvised explosive device (IED) 22A.5.4 Dense inert metal explosives (DIME) 22A.5.5 Landmines and unexploded ordnance (UXO) 23


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Basic principles

Weapons systems can act at a greater and greater distance from the victim.

Explosive devices have become the major weapons deployed in contemporary warfare.

Fragments from explosive devices have become the most common mechanism of wounding.

An open-air bomb explosion consists of three phases: positive-pressure shock wave; negative-

pressure suction wave; and blast wind.

A.1 Short history of the weapons of warand armed conflict

From traditional face-to-face combat using bare fists, sticks and stones, knives, swordsand spears, other “hand-energized” weapons that struck at a distance came intobeing: the sling-shot, javelin and bow and arrow. The invention and propagation ofgunpowder triggered off a revolution in warfare with the development of weapons

that act at an even greater distance: explosive devices and the rifle.The evolution of warfare has in certain respects largely been based on suchtechnological developments that have engendered a wide variety of tacticalcombat situations and greatly affected the numbers of casualties and the types ofwounds incurred.

Advances in the technology of modern high-order explosives and especially theirdelivery systems constitute one of the major factors that allow combatants toovercome more readily the “natural inhibition” against killing fellow human beings.1 2 3 These developments have given rise to an enormous variety of combat scenarios frommassive artillery and aerial bombardment of urban areas to the widespread use oflandmines, the “perfect” remote and indiscriminate weapons that do not even requirethe perpetrator to pull a trigger.

Practically speaking, the result of this evolution has been the change in thepreponderant wounding mechanism in the last 100 years from bullets to fragments or

“shrapnel”, which now cause up to 80 % of the injuries seen in wars between classicalarmies. Guerrilla warfare still results in a higher incidence of gunshot wounds (seeSection 5.5).

Fragments are the result of various explosive mechanisms and systems: aerial bombs,artillery or mortar shells; rocket-propelled and hand grenades; landmines andimprovised explosive devices.

Sections 3.3.6 and 3.4.8 in Volume 1 discuss the wound ballistics of fragments. However,in addition to the production of fragments, explosive devices also have a primary blasteffect that causes lesions with particular characteristics. Part A of Volume 2 is devotedto blast injuries.

1 John Keegan. The Face of Battle. London: Jonathan Cape Ltd; 1976.

2 Lt. Col. Dave Grossman. On Killing: The Psychological Cost of Learning to Kill in War and Society . New York, NY: Little,Brown and Co.; 1995.

3 Joanna Bourke. An Intimate History of Killing: Face-to-Face Killing in Twentieth-Century Warfare. London: GrantaBooks; 1999.

Figure A.1

Collection of various munitions.

I C R C


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A.2 Munition composition

Explosives are described as either high- or low-order and provoke different patternsof injury. Low-order explosives include gunpowder, small bombs such as pipe bombs,and “Molotov cocktails” (petroleum based). High-order explosives can either beimprovised using simple substances available commercially, such as fertilizer anddiesel fuel, or specifically manufactured. The latter can be for civilian use, for examplequarrying, building dams and other large civil engineering projects, or “military-grade”,

and include TNT, dynamite, Penta, and plastic explosive (PE4, C4, Semtex). Munitionsnormally use a combination of specialized high-order explosives.

All munitions contain an explosive train: a series of components that are designedto ensure the explosive charge functions in the required way at the required time.In a gun or rifle it is a low-explosive train, where a primer is struck that produces aflash igniting the propellant contained in the cartridge case. The burning propellantproduces gases in a restricted volume thus causing a high pressure to build up. Thispressure acts on the base of the bullet and accelerates it through the barrel (Figure 3.6).

The high-explosive train in a bomb or explosive device has three basic serialcomponents: the primer or detonator, a booster charge, and a final main charge that

produces the desired effect and is the principal determinant of destructive power.The bomb casing holds the components of the device together. It may be purposelydesigned to break up into projectiles (pre-formed fragments of modern weapons,100 – 500 mg in weight and 2 – 3 mm in diameter) that increase the probability ofhitting a person and are more lethal than ordinary irregular fragments. Otherwise, thecasing breaks up irregularly.

A.3 Open-air bomb explosion

The detonation of an explosive is an exothermic4 chemical process that converts theexplosive charge into high-pressure gases in an extremely short time, measured inmicroseconds.5

In an open-air bomb explosion, part of the energy from the gases produced rupturesthe casing, imparting high kinetic energy to the resulting fragments; their initialvelocity may be up to 2,000 m/s. Another part produces heat in the form of a fireball,as well as sound, light and smoke. The remaining energy causes the gases to expandrapidly, compressing the surrounding air to produce a blast or shock wave – a pressurepulse – that spreads out spherically in all directions from the point of origin. This blastwave expands faster than the speed of sound and has three components.

4 An exothermic chemical reaction converts the energy in chemical bonds into heat, in contradistinction to anendothermic reaction that absorbs heat.

5 For a low-grade combustion, such as occurs with the gunpowder in a bullet cartridge, this process is about200 – 400 m/s, relatively slow. For a high-grade combustion in the case of military munitions, the conversiontakes place at a speed up to 9,000 m/s or more.

Figure A.4

Friedlander curve: pressure-time relationship

of a blast wave in open air without obstacles inits path. The area under the curve is the totalimpulse per unit area.

Positive-pressure shock wave: a pulse of peakoverpressure that travels through the ambientmedium – air, water or the ground. Only high-orderexplosives cause an overpressure shock wave.

Negative pressure or rarefaction phase:a suction wave, again only occurring withhigh-order explosives.

Blast wind: phase of dynamic overpressurewith the mass movement of heated air andcombustion products. This is produced by both

high- and low-order explosives. Time

Peak blast overpressure

Positive pressure

phase

Negative pressure

phase

Atmospheric

pressure

Blast wind

Pressure

I C R

C

Figure A.2

Civilian and military-grade plastic explosives.

I C R C

Figure A.3

Irregular fragment removed from avictim’s body.

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A.3.1 Positive-pressure shock wave

The positive-pressure shock wave is a moving peak of high pressure and densitytravelling at supersonic speed at first, as high as 3,000 – 9,000 m/s, but decreasing veryquickly with distance. It is of very short duration – in the order of milliseconds – but ofvery rapid onset, and reaches its maximum pressure load almost instantaneously. Thishigh-pressure peak, in the order of hundreds of bars,6 also decreases rapidly as thewave moves away from the source of the explosion (inversely proportional to the cube

of the distance). Its leading edge in air is called the “blast front” and is visible becauseof the way it refracts light (Figure A.5). The overpressure of the blast front provokes ashattering effect, also known as brisance. Tissue damage depends on the magnitudeand duration of the peak overpressure: the impulse.

A.3.2 Negative-pressure suction wave

The passage of the positive component is followed by a negative pressure trough, arelative vacuum, which sucks in air and debris. The pressure differential is much lessthan the positive phase, but can last three to ten times as long, and during its firstphase it has more destructive energy than the positive peak.

A.3.3 Blast wind

The rapidly expanding gases from the explosion displace an equal volume of airand, together, produce a blast wind. This mass movement of air creates a “dynamicoverpressure” that travels immediately behind the shock wave, but at a much lowerspeed. Nonetheless, it can reach several hundred km/h (approximately 100 m/s). Itis of lower amplitude than the shock wave, but lasts much longer and travels muchfurther. This dynamic overpressure knocks over or scatters any object shattered by thebrisance effect of the shock wave.

A.4 Effects due to the environment

The propagation of the blast wave can become very complicated in the presence ofobstacles or when channelled along streets, corridors, or through pipes and tunnels.Like sound waves, a blast shock wave flows over and around an obstacle and will affectsomeone sheltering behind. On the other hand, obstacles can also create blast waveturbulence immediately behind them with the formation of relatively safe areas, whichis why sometimes people close to explosions survive with relatively minor injuries,or none at all, while those further away suffer more serious injuries or are killed. Thewearing of body armour protects against penetration of fragments but not against theoverpressure shock wave.

Blast waves hitting a wall perpendicularly exert much greater pressure than those

hitting surfaces at an angle. In addition, the perpendicular wave is compressed andreflected back by the wall, causing an amplification of the waves and creating a regionof more intense pressure. Thus, a blast in an enclosed or confined space (building,bus, etc.) results in additive reflections of the pressure wave rebounding off the walls;the amplified overpressure is much higher and the impulse lasts longer (Figure A.6).This has an important influence on mortality and on the severity of injury among thepeople inside. In addition, an explosion in an enclosed space increases the likelihoodof the building collapsing.

In underground and underwater explosions the shock wave travels more rapidly andmuch further because sound has a higher velocity in the denser medium. The radiusof lethal injury is about three times greater in water explosions than in air, and injuries

at the same distance are more severe.

6 In physics the correct term is Newton per m2, which has its own unit, the Pascal. In ballistics and meteorology,the term bar is used. One bar equals 100 kilopascals and is approximately equal to atmospheric pressure at sealevel. In non-scientific layman’s language, this is the equivalent in this specific case of hundreds of kg/cm2.

7 Harrisson SE, Kirkman E, Mahoney P. Lessons learnt from explosive attacks. J R Army Med Corps 2007; 153:278 – 282.

Figure A.5

Explosive detonation. Note the blast frontindicated by the arrow.7

C r o w

n C o p y r i g h t

Time

Atmospheric

pressure

Positive pressure phase

Blast overpressure

Pressure

Figure A.6

Typical pressure – time relationship of a blast inan enclosed space.

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A.5 Specific explosive devices

A number of variations on basic ordnance have been developed to fulfil specificmilitary demands. A short, non-exhaustive list follows.

A.5.1 Enhanced-blast explosive devices

With a thermobaric or fuel-air weapon a first small detonation spreads out explosive

material as a fine aerosol that mixes with atmospheric oxygen, which is then triggeredto produce a second explosion. The disseminated explosive aerosol creates a muchlarger area of propagation of the shock wave and the initial overpressure lasts longerand reaches further than in an ordinary explosion. In addition, the consumption ofatmospheric oxygen in the explosion causes death by asphyxiation. There are fewsurvivors within the range of the primary blast.

A.5.2 Shaped-charge explosives

In these weapons, the explosive device is constructed in such a way as to amplify theblast overpressure and brisance effect and to channel it into a tight trajectory. Theblast wave thus extends as a cone rather than as a sphere starting from a point. The

blast overpressure has a devastating effect within the cone, but very little damage iscaused outside it. One type of anti-tank mine (ATM) is equipped with a shaped charge.

An explosively-formed projectile is a particular type of shaped charge incorporatinga disc that is deformed on detonation into an aerodynamically efficient metal slugthat can go through armour. Such projectiles are used in manufactured ATM and,increasingly, have been deployed as improvised “roadside bombs” against tanksand armoured personnel carriers. Once they break through the armour they causedevastating wounds in the individuals they hit, with relatively minor blast injury tothose nearby.

A.5.3 Improvised explosive device (IED)

As the name implies, these are home-made bombs. The explosive material may bemilitary munitions (mortar or artillery shells, or landmines) or commercially availableproducts. IED are used by insurgent groups and non-State actors and factions, andinclude a great diversity of types, small and large, and are more-or-less efficient: pipebombs, car bombs, roadside bombs, booby-traps, etc.

A.5.4 Dense inert metal explosives (DIME)

This device mixes tiny particles of an inert heavy metal, such as tungsten, together withthe explosive; thus the fragments are incorporated into the explosive itself rather thanderived from the casing, which is made of a material with little fragmentation effect.The result is the creation of a shower of “microfragments” on detonation producing anincreased brisance from a relatively low initial blast yield. These microfragments arehighly lethal at close range, but the effects fall off very rapidly and the lack of casingfragmentation limits injury to others nearby. Survivors typically present traumaticamputations or severe soft-tissue injuries and retained heavy metal dust, which maybe a source of toxicological concern.8

8 The data concerning the toxicity of tungsten is limited and contradictory and mostly confined to chronicexposure. Acute intoxication is rare but may present with nausea and the sudden onset of seizures, coma andencephalopathy, and acute tubular necrosis. Carcinogenic potential is a possibility. Treatment is supportive andsymptomatic. Please see Selected bibliography.

Figure A.7

Disc incorporated into anexplosively-formed projectile.

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A.5.5 Landmines and unexploded ordnance (UXO)

A landmine constitutes a particular explosive device that is legally defined by themethod of activation. Whether industrially-manufactured or improvised, a mine isactivated by the victim. An anti-tank or anti-vehicle mine is “designed to be detonatedor exploded by the presence, proximity or contact … of a vehicle “.9 An anti-personnelmine is defined as “designed to be exploded by the presence, proximity or contact ofa person”.

Anti-personnel mines have been banned by an international convention, which haschanged the military doctrine of many countries.10 Nonetheless, APM continue tobe used during some conflicts, albeit far less frequently and in far smaller quantitiesthan before.

Other unexploded ordnance and abandoned explosive ordnance also litter battlefieldslong after combat has ceased: these are the infamous explosive remnants of war(ERW).11 Cluster munitions “release explosive submunitions each weighing less than20 kilograms”,12 which in many cases do not explode as they should and constitute aform of UXO. The same can be said of booby-traps.13

Observers and data collection systems are usually not capable of distinguishingbetween different types of mines and UXO, and all these weapons constitute a dangerfor civilian populations and clearance experts well after the cessation of hostilities.The mechanism of injury and clinically important sequelae are the same for bombs,landmines and UXO.

Chapter 19 deals more broadly with the primary blast effects of explosions and expandson Section 3.1.4. Chapter 20 considers anti-tank mines, while Chapter 21 developsSection 3.1.3 and discusses in detail the specific example of anti-personnel landmines.

9 Convention on Prohibitions or Restrictions on the Use of Certain Conventional Weapons which May beDeemed to be Excessively Injurious or to Have Indiscriminate Effects, Protocol II on Prohibitions or Restrictionson the Use of Mines, Booby-Traps and Other Devices. Geneva, 10 October 1980, as amended on 3 May 1996.

10 Convention on the Prohibition of the Use, Stockpiling, Production and Transfer of Anti-Personnel Mines and ontheir Destruction, 18 September 1997. As at 31.12.2012, there were 160 States Parties to this Convention.

11 Protocol on Explosive Remnants of War (Protocol V to the 1980 Convention), 28 November 2003.

12 The Convention on Cluster Munitions, 30 May 2008, has banned the use of cluster ammunitions. As at31.12.2012, there were 77 States Parties to this Convention.

13 “Booby-trap” is defined as “any device or material which is designed, constructed or adapted to kill or injureand which functions unexpectedly when a person disturbs or approaches an apparently harmless object orperforms an apparently safe act”, according to the 1980 Convention on Conventional Weapons (Protocol II).

Figures A.9.1 – A.9.3

Cluster munitions.

I C R C

M .

B a l d a n / I C R C

M .

B a l d a n / I C R C

Figure A.8

Unexploded ordnance.

M .

K o k i c /

I C R C


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Chapter 19

EXPLOSIONS

AND PRIMARY BLASTINJURIES


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19. EXPLOSIONS AND PRIMARY BLAST INJURIES

19.1 Introduction 27

19.2 The single bombing incident 27

19.3 Epidemiology 2919.3.1 Mortality 2919.3.2 Survivors 31

19.4 Pathogenesis and pathophysiology 3219.4.1 Primary blast injury: barotrauma 3219.4.2 Secondary blast injury: fragment wounds 3419.4.3 Tertiary blast injury: blast wind 3419.4.4 Quaternary or miscellaneous blast injury 34

19.5 Clinical presentations and management 3419.5.1 General concussion syndrome: resistance to resuscitation 3519.5.2 “Shell shock” and the “bewildered” walking wounded 35

19.6 The ear and ruptured tympanum 3619.6.1 Management 36

19.7 Blast lung 3619.7.1 Clinical presentations 3619.7.2 Chest X-ray and pulse oximetry 3719.7.3 Assessment of patients with suspected lung injury 3819.7.4 Patient management 38

19.8 Arterial air embolism 39

19.9 Visceral injury 39

19.10 Eye and maxillo-facial injuries 40

19.11 Other injuries 40

19.12 Removal of unexploded ordnance 40


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19

Basic principles

A single explosion can produce many victims suffering a variety of injuries.

A single victim may present all four types of blast injury; fragment wounds usually predominate.

Few casualties survive significant primary blast injury.

Deafness should be suspected in confused or unresponsive patients.

Blast lung can develop insidiously up to 48 hours after exposure and is often fatal.

19.1 Introduction

Explosions can be caused by various events.

• Physical-mechanical: exploding pressure cooker.

• Exothermic chemical: conventional military-type explosion transforming a chemicalcompound – solid or liquid – into a large quantity of gas in an exothermic reaction,

as seen in bombs, shells, mines and incendiary bombs (napalm, white phosphorus).

• Nuclear: fission or fusion device, atomic and hydrogen bombs.

Non-conventional chemical weapons may or may not involve a conventional detonationthat bursts open a container spreading out a toxic chemical substance. A radiologicaldispersal device, a so-called “dirty bomb”, works in the same way, with a conventionalexplosive surrounded by radioactive material that is spread out by the explosion; it is nota nuclear device. This chapter deals only with conventional weapons.

Explosive devices have been given different names, usually indicating the meansof delivery: letter, pipe, car or aerial bomb; artillery or mortar shell; cruise missile;hand grenade and rocket-propelled grenade; and landmine. Some, such as militaryammunition, are industrially manufactured; others are “home-made” and areknown as improvised explosive devices. Whether an explosive device is industriallymanufactured or improvised makes little qualitative difference in the physics of theexplosion and the clinical results of its blast effects.

See also Section 3.1.4.

Most of the clinical discussion of this Chapter pertains to primary blast injury.

19.2 The single bombing incident

The great difference between the individually-held assault rifle and an explosivedevice is in the number of victims that can be produced by a single combatant duringa single incident. The range of scenarios using explosive devices during armed conflict

is thus far more varied than with simple firearms, and injuries due to the different blasteffects of explosions have become more common in modern warfare. However, fewsingle bomb explosions have a preponderance of primary blast effects (USS BattleshipCole in Aden harbour, 2000, was one recent example of this).

Blast injuries are commonly categorized into four types

1. Primary, due to direct pressure effects.

2. Secondary, due to fragment projectiles.

3. Tertiary, due to the blast wind.

4. Quaternary, or miscellaneous: burns, toxic gases, etc.


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In wartime, most medical services and facilities – whatever the level of resources –are prepared and expect the arrival of large numbers of casualties, which they dealwith to the best of their capabilities. Even the civilian population learns to takecertain protective measures and violence is expected. However, the single bombingincident in an urban environment, taking the system by surprise, results in a numberof characteristic problems. General confusion reigns: there is often panic and hysteriaamong survivors and bystanders. Coordination and communication betweenarmed forces or militias, police, fire-fighters, and first-aid or paramedical teams and

ambulances are usually insufficient. In addition, the lines of communication are oftencut or overburdened and become non-functional.

If there is structural collapse of a building, delayed rescue and evacuation of patientswith a heavy death toll is common. Injuries may also occur among rescuers. Evacuationof most casualties is done by private means: taxis, private cars, or manually-bornestretchers, in a crowded urban environment where the streets are blocked by roadtraffic. The closest hospitals are invariably flooded with the early arrival of patientswith relatively minor wounds: the “reverse triage” phenomenon (see Sections 7.7.8and 9.13).

Most fatalities are immediate and located at the scene. About one half of all thesurvivors arrive at hospital within the first hour, giving an approximate indicationof the total number of wounded. Most survivors, however, are not severely injuredand the majority can be treated as outpatients. Late neurological and psychologicalsequelae among survivors are common and may overlap with the signs and symptomsof post-traumatic stress disorder (PTSD).

The limbs, head and neck are the most commonly injured areas, particularly in people

who are only superficially wounded. Only about 10 % of the survivors admitted tohospital have critical injuries.

Figure 19.2

Building collapse: the frequent result ofa bombing.

M a g n u m / C .

A n d

e r s o n / I C R C

Figure 19.1

Fireball and plume of dust and smoke arisingfrom a bombing.

M .

D e l l a T o r r e / I C R C


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19.3 Epidemiology

The general epidemiology of armed conflict as described in Chapter 5 applies. Mostwar wounds are the result of fragments from some sort of explosive device, but mostwounded survivors have been injured beyond the radius of the primary blast effect.Indeed, within this radius the density of primary and secondary fragments is so greatthat lethal injuries are caused by both primary blast effect and fragments. However,many different tactical situations exist. This section describes some epidemiological

observations from single bomb explosions where casualties are close enough for allfour mechanisms of injury to come into play.

With bomb explosions there is a potential for multiple casualties and multiple woundsin the same patient. Most explosions create mixed injuries with fragment injuriespredominating. The number of casualties and the ratio of different kinds of injuriesare determined by a number of factors:

• power of the explosion (magnitude and duration of peak overpressure);• distance of people from the blast point and their degree of personal protection;• environmental conditions of the spread of the blast wave

– topography and relief of the terrain; – presence of buildings and other obstacles; – meteorological conditions; – confined space; – presence of water;1

• tactical situation – crowded street or market place, or other public space, etc.

19.3.1 Mortality

Casualties may suffer total body disruption or fireball carbonization. Some bodies mayshow no recognizable external sign of penetrating or blunt injury – there are manyanecdotal reports from World Wars I and II of dead soldiers found on the battlefieldwithout any external signs of injury.

1 People who are partially submerged in water when subjected to a blast explosion, for example, suffer verydifferent injuries to the under-water and above-water body parts.

2 French physiologist who was the first to correctly determine the expansion of gas as the primary effect of a blastexplosion. Cited in Hill JF. Blast injury with particular reference to recent terrorist bombing incidents. Ann R CollSurg Engl 1979; 61: 4 – 11.

Blast event: multiple mechanisms, multiple casualties,multiple body regions hit.

“La mort était due à la grande et prompte dilation [sic] d’air.”

(Death was caused by the great and immediate expansionof air.)

Pierre Jars 2 1758

Figure 19.3

Total body carbonization of a mother and twochildren following a bomb explosion.

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Table 19.1 gives a short list of various contemporary single bomb incidents and thedifferent tactical situations: open space, confined space, “ultra-confined” space of abus, building collapse, etc.

Event TypeImmediatedeaths (%mortality)

InjuredHospitalized

(%)Critically injured* (%)

Criticalmortality

(%)Remarks Reference

Bologna railwaystation, Italy,

1980.

Confined space;partial building

collapse.

73 (25 %) 218 181 (83 %) 25 (10 %) 11 (44 %)Partial collapse with

stones from the building as

secondary missiles.

Brismar &Bergenwald,

1982.

Beirut USMarine barracks,Lebanon, 1983.

Open air, largebomb; building

collapse.234 (68 %) 112

86 (77 %)referred onward.

19 (17 %) 7 (37 %) All evacuated to ship.Frykberg &

Tepas, 1989.

Paris metro,France,1985 – 86.

Confined space;small home-

made bombs.13 (5 %) 255 205 (80 %) 40 (16 %) 7 (18 %)

Large number of severelyinjured; small blast in

crowded confined space.

Rignault& Deligny,

1989.

Civilian busJerusalem,Israel, 1988.

Small confinedspace; bus

windows closed.Bomb inside bus.

3 (5 %) 55 29 (53 %) 8 (31%) 3 (37.5 %)

High rate of primaryblast injuries: perforated

ear drums 76 %; blastlung 38 %; abdominal blast

injuries 14 %.

Katz et al.,1989.

Federal BuildingOklahoma City,USA, 1995.

2,000 kg bomb

fertilizer + fueloil. Open space,

building collapse.

166 (21 %) 592 83 (14 %) 52 (9 %) 5 (10 %)

Fatalities primarily incollapse zone: out of 361inside building 163 dead

(45%) and 156 injured (88%of total casualties).

Teague,

2004 &Mallonee

et al., 1996.

USS BattleshipCole, Adenharbour, Yemen,2000.

Confined space;no collapse of

superstructure;efficient

fire-fighting.

16 (30 %) 39 All evacuated. 11 (27 %) 1 (9.1 %)

All dead had severeorthopaedic injuries; 64% of

survivors had orthopaedicinjuries; peripheral woundthrombosis up to 72h later.

Langworthyet al., 2004.

Khobar Towers,Saudi Arabia,2001.

20 kg bomb;open space;

building collapse.19 (5 %) 555 66 (16 %) 24 (6 %) 0

Fatalities: multiple blunt,glass and foreign body

injuries; 27 % injured duringrescue and evacuation

or clean-up.

Thompsonet al., 2004.

Shoppingcentre Helsinki ,Finland, 2002.

Open space. 5 (4%) 161 66 (41%) 13 (20%) 1 (8%)(1 DOA**)

Efficient pre-hospital anddispatch system.

Torkki et al.,2006.

Suicide carbomb Karachi,Pakistan, 2002.

Small confinedspace. Bombnext to andbelow bus.

24 (67%) 11 11 (100%) 2 (18%) ***

11/12 survivors withfracture / dislocation

calcaneus and bones of foot:" pied de mine" effect.

Zafar et al.,2005.

Israel2002 –2003.

5 bus bombings. 56 (21 %) 208 121 (58 %) 17 (8 %) 0Most lethal: bus is defined as

an “ultra-confined space”.

Kosashviliet al., 2009.

3 closed-spacebombings

(restaurant, etc.).52 (17 %) 256 101 (40 %) 35 (13 %) 9 (2.9 %) Relatively lethal scenario.

4 open-spacebombings.

26 (8 %) 305 120 (39 %) 25 (8 %) 5 (1.5 %) Least lethal scenario.

Madrid trainbombing, Spain,2004.

Confined space. 177 (8.6 %) 2,062 512 (25 %) 72 (14 %) 14 (19.5 %)

Large numbers withsuperficial injuries andemotional shock: not

hospitalized but burdenon triage.

Turégano-Fuentes

et al., 2008.

Londontransportbombings:3 undergroundtrains + 1 bus,UK, 2005.

Confined space,small explosions.

53 (7 %) 722 667 20 (3 %) 3 (15 %)

Good pre-hospital triage.Large number of walking

wounded neverthelesshospitalized.

Aylwin et al.,2006.

* Injury Severity Score (ISS) > 15.

** DOA: dead on arrival.

*** Victims were French engineers; evacuated within 24 hours by order of French authorities.Table 19.1 Major contemporary single bomb incidents: a partial list. References are to be found in the Selected bibliography.


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Explosions with very high rates of immediate death have certain characteristics,whatever the source or means of delivery (car bomb, aerial bombardment, etc.):• very powerful explosion – the larger the bomb, the greater the destructive effects;• explosion in a confined, closed space – mortality can reach 50 % or higher;• building collapse – very few survivors amongst those crushed and trapped by

the rubble;• ignition of secondary fires.

Explosions in confined spaces are particularly devastating, with an overall highermortality rate. Survivors have more severe injuries with a higher incidence of primaryblast injuries, including a predominance of blast lung and burns affecting a large bodysurface area.3

Most fatalities present multiple trauma and are due to total body disruption, injuriesto the skull and brain, rupture of one of the solid abdominal organs, blast lung andtraumatic amputation.4

Most bombings, however, generate a large number of casualties with relativelysuperficial wounds that do not require hospitalization, as shown in Table 19.1.Accurate and efficient triage permits quick identification and treatment of severely-injured patients, thus lowering the critical mortality rate.5

19.3.2 Survivors

Amongst survivors, as is the case with other weapons systems, most injuries due toexplosive blast and requiring surgery involve the limbs. Up to 85 % of hospitalizedpatients have musculoskeletal injuries.

Many patients suffer multiple injuries caused by a wide variety of blast effects, coveringa whole spectrum of trauma. Representative of this are the injuries recorded followingthe bomb attacks against the Madrid trains in 2005; only 512 patients among morethan 2,000 casualties were deemed seriously injured enough to be recorded in thisstudy (Table 19.2).

Body region Patients wounded Injuries

Head, neck and face

Brain and skull

Neck

Tympanic perforation

Eye injuries

Maxillo-facial fractures

Other face

340

41

8

240

95

48

14

Chest 199

Abdomen 28

Limbs 71

External

Shrapnel wounds: non-penetrating

Burns

263

211

89

Table 19.2 Distribution of injuries according to body regions, Madrid railway bombings 2005.6 Patients with

superficial bruises, transient hearing loss, and/or emotional shock only were excluded. Many

patients suffered more than one injury; therefore, the total number of injuries exceeds the

number of patients.

3 Leibovici D, Gofrit ON, Stein M, Shapira SC, Noga Y, Heruti RJ, Shemer J. Blast injuries in a bus versus open-airbombings: a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma 1996; 41: 1030 – 1035.

4 Hill JF. Blast injury with particular reference to recent terrorist bombing incidents. Ann R Coll Surg Engl 1979; 61:4 – 11.

5 The critical mortality rate concerns patients with an Injury Severity Score greater than 15.

6 Adapted from Turégano-Fuentes F, Caba-Doussoux P, Jover-Navalón JM, et al. Injury patterns from major urbanterrorist bombings in trains: the Madrid experience. World J Surg 2008; 32: 1168 – 1175.


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19.4 Pathogenesis and pathophysiology

Although four different categories of blast injury are described, they often coexist ina single patient.

19.4.1 Primary blast injury: barotrauma

Primary blast injuries are due to the direct effects of over- and under-pressure caused

by the shock wave: i.e. barotrauma. These injuries are usually confined to a relativelysmall area around the point of explosion.

The peak overpressure induces surface compression and deformation waves uponhitting the body and interacts with the tissues to produce two types of energy: stressand shear waves.

A stress wave passes longitudinally through the tissues. When it reaches a planebetween two tissues of differing density part of it is reflected and part continues,creating pressure differentials. These are particularly acute at air-solid (e.g. ear), air-fluid (e.g. hollow viscera, lung alveoli) and fluid-solid interfaces of delicate structures(e.g. blood vessels).

The air-fluid interface is exceptionally sensitive. The positive pressure stress waverapidly compresses air in any isolated pockets. With the negative pressure phasethe air re-expands violently, rupturing the surrounding tissues. This causes spalling,presenting an effect much like that of air bubbles in boiling water.

Shear waves propagate transversely to tissue interfaces, similar to the decelerationforces seen in a motor vehicle collision. Contiguous tissues with different densitiesare accelerated and decelerated at different rates creating a shearing actionthat overstretches natural tissue elasticity and causes tearing and disruption ofattachments. This is especially prominent in solid organs and organs with an elasticanatomic fixation, such as the mesentery of the bowels, the tracheo-bronchial tree orthe placenta.

Primary blast effects include specific injury to various parts of the body.

Ear

Rupture of the tympanic membrane is the most common injury , but does not dependonly on the absolute blast overpressure. The orientation of the head, i.e. the externalauditory canal acting as a corridor for the passage of blast pressure, is an importantconsideration. Transitory sensorineural deafness (neurapraxia of the receptor organs)is very frequent. Degloving of the cartilage of the external ear may also occur.

Lung

Lung injuries carry the highest morbidity and mortality . The alveolar-capillary septumis the typical air-fluid interface where spalling may occur. Alveolar air is compressed

by the positive pressure wave and, with the negative phase, the alveoli burst. Inertialshearing occurs at the attachments of the tracheobronchial tree.

The disruption of peripheral alveoli may lead to the formation of subpleuralcysts and tearing of the visceral pleura. Pneumothorax, haemopneumothorax,pneumomediastinum and/or surgical emphysema may result.

The increase in air pressure in the alveoli, above that of the fluid pressure in thevascular tree, produces rupture of this membrane with intra-alveolar haemorrhageand oedema, and alveolar-venous fistulas; the negative pressure phase may inducesystemic air emboli.


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The resultant oedematous and haemorrhagic lungs (hepatization or “wet lung”syndrome) are stiff and heavy: up to 2 – 3 times their normal weight. As in bluntinjury to the lungs, alveolar haemorrhage and oedema cause ventilation-perfusiondisequilibrium (intrapulmonary shunt) and decreased lung compliance, resulting inhypoxia and greater effort to breathe.

Furthermore, the positive pressure wave can deform the bony thoracic cage causingfractures of the ribs that may lacerate the lungs or compress the lungs between thesternum and vertebral column resulting in direct pulmonary contusion, characterizedby the haemorrhagic stripes on the lung surface.

Hollow viscera

Any perforation due to the direct effect of the pressure wave is usually immediate andmost commonly affects the ileo-caecal region or colon.

Less common are delayed perforations that develop insidiously in stages owing toa process of intramural haemorrhage and/or mesenteric ischaemia, both leading toinfarction, necrosis and gangrene of the affected site. Pathological studies on rats haveshown the injury to begin in the mucosa and then migrate toward the serosa.8 Necrosisbegins 6 hours after injury and perforation after 48 hours, usually occurring betweenday 3 and 5 in human clinical studies. As a consequence, and unlike projectile injury,any serosal injury due to primary blast seen at operation indicates that the entireintestinal wall is involved and requires debridement and repair.

Solid organs

Ischaemia, infarction or haemorrhage often occur; complete rupture of the liver,spleen or kidney is rarely seen in survivors.

Musculoskeletal system

Brisance can fracture long bones; the blast wind that follows the shock wave then

strips away the soft tissues. One possible result in victims close to the blast epicentre istraumatic amputation, which usually occurs at the upper third of the tibia. Abdominalevisceration is also seen. Massive soft-tissue wounds are frequent.

Eye

Rupture of the eye globe and open fracture of the orbital ridge are possible.

Head and central nervous system

Direct blast overpressure causes diffuse axonal injury, and coup-counter-coup injuryas well as fractures of the skull. Petechial haemorrhages with brain oedema are seen.Cerebral vasospasm that can last for up to a month may occur and some authors havereported pseudoaneurysms of the cerebral vessels following the vasospasm.

Pathological changes of secondary neurodegenerative effects at the molecular andcellular levels may continue for hours or even days after exposure. Various metabolic

7 Adapted from Hill JF, 1979.

8 Tatic V, Ignjatovic D, Jevtic M, Jovanovic M, Draskovic M, Durdevic D. Morphologic characteristics of primarynonperforative intestinal blast injuries in rats and their evolution to secondary perforations. J Trauma 1996;40 (Suppl.): S94 – S99.

Figure 19.4

Alternating phases for lung haemorrhage andvascular air emboli.

Normally, the intravascular fluid pressure isgreater than the air pressure in the alveoli. Thisintravascular pressure reacts less to the changesdue to blast than the alveolar air.

With peak pressure, the alveolar-capillary

membrane ruptures and intravascular fluidenters the alveolar space: fluid to gas phasecausing “forced” haemorrhage and oedema.

With negative pressure, intra-alveolar air ispressed into the capillaries: gas to fluid phasecausing “forced” air embolization.7 Time

Gas pressure

Fluid pressure

External pressure(sustained)

Maximum compression

of thorax

Pressure

Figure 19.5

Traumatic amputation of the lower legs throughthe tibia.

M .



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and neuroendocrine effects as demonstrated by certain biochemical markers havebeen observed.9 10 11 Late residua have been reported in survivors with even mild braintrauma and can prove debilitating.

Autonomic nervous system

The blast wave can stimulate the pulmonary C-fibre receptors of the vagus nervelocated in the alveolar septa, thus activating the “pulmonary defensive reflex” ofa pronounced vagal state: a triad of apnoea, bradycardia and hypotension. The

result is the paradoxical condition of profound shock with bradycardia, rather thancompensatory tachycardia, as well as the absence of compensatory peripheralvasoconstriction. A loss of skeletal muscle tone is also a feature of this vagalnerve-mediated response, which can reach extreme levels of temporary flaccid orspastic paralysis.12 13

19.4.2 Secondary blast injury: fragment wounds

Projectiles may be primary fragments, derived from the casing or bomb contents, orsecondary missiles: objects mobilized by the blast wind or arising from environmentaldebris (glass shards from shattered windows, wood splinters, soil and stones).

Fragment wounds within the radius of the primary blast effect result in more severe

injuries; the cavitation effect described for projectiles is compounded by blast-drivendebris and delayed thrombosis of small vessels.

19.4.3 Tertiary blast injury: blast wind

The blast wind can displace people, throwing them against objects, or mobilize largeobjects in the environment which then strike people, causing blunt trauma. Brisanceand the blast wind can cause building collapse with subsequent entrapment andcrush injuries as well as head trauma, traumatic asphyxia, fractures and spinal injury.

19.4.4 Quaternary or miscellaneous blast injury

The fireball of the explosion may reach 3,000° C causing flash burns; it may also set fireto the environment, as when a building goes up in flames. Most affected are the faceand hands because clothing offers some protection, although it often also catchesfire. The combination of blast effect and a burn injury affecting more than 30 % bodysurface area is usually fatal.

The blast can let off toxic gases, including carbon monoxide, leading to asphyxia.Inhalation of dust, smoke and other contaminants can also affect respiration.

19.5 Clinical presentations and management

Most patients suffer from a combination of the four blast injury mechanisms. Theclinical presentation and basic management of soft-tissue fragment wounds arecovered in Chapters 10 and 11 and those of specific anatomic regions are the subjectof the remaining chapters of this Volume. This section describes only primary blastinjury. Pure primary blast injury is rare, except from explosions in an extremelyconfined space, as well as underwater and fuel-air explosions. The environment andthe particulars of the event should alert the surgeon to the possibility of primaryblast injury.

9 Cernak I, Savis J, Ignatovic D, Jevtic M: Blast injury from explosive munitions. J Trauma 1999; 47: 96 – 104.10 Cernak I, Savic J, Zunic G, Pejnovic N, Jovanikic O, Stepic V. Recognizing, scoring, and predicting blast injuries.

World J Surg 1999; 23: 44 – 53.

11 Cernak I, Wang Z, Jiang J, Bian X, Savic J. Ultrastructural and functional characteristics of blast injury-inducedneurotrauma. J Trauma 2001; 50: 695 – 706.

12 Guy RJ, Kirkman E, Watkins PE, Cooper GJ. Physiologic responses to primary blast. J Trauma 1998; 45: 983 – 987.

13 Irwin RJ, Lerner MR, Bealer JF, Mantor PC, Brackett DJ, Tuggle DW. Shock after blast wave injury is a vagallymediated reflex. J Trauma 1999; 47: 105 – 110.

Figure 19.6

X-ray showing glass shards in the tissues.

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19.5.1 General concussion syndrome: resistance to resuscitation

Russian surgeons in Afghanistan and, more recently, US surgeons in Iraq andAfghanistan have described patients with mixed patterns of blast injury, largely dueto anti-tank and anti-personnel landmines in the first case and improvised explosivedevices in the latter. Separated by over twenty years, the clinical descriptions areeerily similar.

The condition manifests itself clinically as haemorrhagic shock that is resistant to

aggressive fluid resuscitation after haemorrhage control. Hypotension may beconstant or recurrent after a temporary positive response, but haemodynamic stabilitycannot be maintained. Mortality is high.14

The cause has been ascribed to a combination of barotrauma to the central andautonomic nervous systems and hormonal and metabolic changes, including theinflammatory cascade. The condition may be so severe that some authors have spokenof a “general concussion syndrome”.15 16

19.5.2 “Shell shock” and the “bewildered” walking wounded

Survivors of the sudden flash, sonic boom and neural barotrauma of an explosion

can experience what was once called “shell shock”. Wind of shot, vent du boulet ,soldier’s heart, combat fatigue, reflex paralysis, air concussion, shell concussion, blastconcussion,17 are all terms that were used in the past to describe similar conditions

– nowadays they would be considered extreme forms of PTSD.

The patient appears disorientated and dazed and does not respond well to questionsduring the clinical examination in spite of having an intact eardrum. However, mildblast neurotrauma may also be combined with a defect in hearing. In a civilianpopulation subjected to an isolated bombing event there is probably also a subjectivepsychological element of horror, fear and disorientation – “psycho-emotional shock” –in addition to physiological somatic changes.

Bradycardia and hypotension may set in and persist in the absence of an obviouscause. Severe cases can go into convulsions or paralysis, including paraplegia. Apossible extreme vagal state may even be falsely diagnosed as death: very slow pulse,unrecordable blood pressure, very slow respiration or even absence of respiratory effort.

Most such signs and symptoms are usually transient and resolve in minutes tohours after exposure. Observation for four to six hours after blast exposure isusually sufficient. Management is conservative and supportive: maintaining goodoxygenation and observation of the patient for any signs of increased intracranialpressure. Physical effort should be minimal during recuperation with a gradual returnto everyday activities; treatment is symptomatic, e.g. paracetamol for headache. Long-term neurological and psychological effects are common.

14 Nelson TJ, Clark T, Stedje-Larsen ET, Lewis CT, Grueskin JM, Echols EL, Wall DB, Felger EA, Bohman HR. Closeproximity blast injury patterns from improvised explosive devices in Iraq: a report of 18 cases. J Trauma 2008;

65: 212 – 217.15 Nechaev EA, Gritsanov AI, Fomin NF, Minnullin IP, eds. Mine Blast Trauma: Experience from the War in

Afghanistan. St Petersburg: Russian Ministry of Public Health and Medical Industry, Vreden Research Instituteof Traumatology; 1995. [English translation: Khlunovskaya GP, Nechaev EA. English publication: Stockholm:Council Communications; 1995.

16 Bryusov PG, Shapovalov VM, Artemyev AA, Dulayev AK, Gololobov VG. Combat Injuries of Extremities. Moscow:Military Medical Academy, GEOTAR; 1996. [Translation by ICRC Delegation Moscow]

17 Various denominations and references cited in Clemedson C-J. Blast injury. Physiol Rev 1956; 36: 336 – 354.

The incidence of mild blast neurotrauma is probablygreatly underestimated.

Figure 19.7

The walking wounded: dazed, disoriented,and frightened.

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19.6 The ear and ruptured tympanum

Almost all persons closely exposed to a significant blast suffer functional perceptivedeafness and some dizziness at the time of the explosion; the inner ear can sufferdamage at a pressure insufficient to rupture the tympanum. Most recover rapidly witha return to normal hearing within a matter of minutes or hours.

Apart from transient sensorineural deafness and dizziness, perforation of the tympanic

membrane is the most common organic injury and occurs at the lowest blast pressures.It is rare for a casualty to have an intact tympanum yet suffer other serious injury. Anotoscopic examination on its own, however, is insufficient to rule out the possibility.Consequently, the otoscopic examination must be assessed in correlation with othersigns and symptoms, particularly of the respiratory system, to determine which patientsrequire continued observation in hospital.

Please note:

In a mass casualty situation, amidst the inevitable confusion, the performance of anotoscopic examination is not a simple procedure to carry out in the emergency room.The ear should be kept clean and dry until proper assessment is possible.

Rupture of the tympanic membrane is manifested by deafness, tinnitus, otalgia, and eardischarge. The surgeon may have to resort to writing notes in order to communicatewith the patient.

19.6.1 Management

Dazed but stable patients with a ruptured eardrum do not require a chest X-ray,providing there are no respiratory symptoms or other clinically significant injuries.They should however be observed for four to six hours.18

Initial treatment of a ruptured tympanic membrane is conservative (see Chapter 28).Most heal spontaneously.

19.7 Blast lung

The lungs are the second most commonly injured organ following exposure to primaryblast, but the leading cause of late blast mortality. The diagnosis of blast lung injury(BLI) is made on a clinical basis and confirmed by chest X-ray.

19.7.1 Clinical presentations

There are three major clinical presentations of respiratory insufficiency in blast victims.

1. Severe respiratory distress with bloody, frothy sputum and rapidly deterioratinglevel of consciousness shortly after exposure, often within minutes.

The condition is immediately life-threatening and the prognosis grave whateverthe treatment. In a mass casualty situation where resources are limited, thesepatients are classed as “expectant” (Category IV ).

2. Progressive respiratory insufficiency developing insidiously over time, oftenwith a full-blown picture only after 24 – 48 hours, and resembling pulmonarycontusion from blunt trauma.

18 Ashkenazi I, Olsha O, Alfici R. Blast injuries: letter. N Engl J Med 2005; 352: 2651 – 2652.

An otoscopic examination on its own is insufficient to ruleout other serious injury, but should be conducted for allblast victims including the unconscious.


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The patient may present at first with mild haemoptysis or persistent cough,and progresses to dyspnoea and tachypnoea with air hunger and cyanosis,tachycardia and hypotension. Moist crepitations are heard in both lung fields.Blood may be found in the endotracheal tube or naso-gastric tube aspirate andpetechial haemorrhages seen in the walls of the larynx. Particular attentionshould be paid to the oxygen saturation by pulse oximetry; a decrease is an earlysign of BLI. The condition can rapidly evolve to a fatal outcome and is the majorcause of delayed deaths.

3. Late development of acute respiratory distress syndrome (ARDS) due to amixture of physiological insults from multiple pathologies: primary blast,inhalation of smoke and toxic gases, hypoxia, haemorrhage and resuscitationwith large quantities of crystalloids and coagulopathy, sepsis, fat embolism, etc.

Signs of pneumothorax, haemothorax, pneumomediastinum (retrosternal crepitus onpressure) and surgical emphysema should be sought in all cases.

19.7.2 Chest X-ray and pulse oximetry

Any patient subjected to explosive blast and suffering the slightest respiratory sign orsymptom, should have a radiograph taken of the chest and be held under observation

for 4 – 6 hours, including pulse oximetry.

The first X-ray may be clear because clinical symptoms appear before radiological signs.Patients with a normal X-ray, but still showing clinical signs or symptoms of pulmonaryeffects after 6 hours, should have a repeat X-ray performed and remain hospitalizedunder observation.

Positive X-ray findings are usually observed within 4 hours if there is BLI and showas pulmonary opacities: infiltrates that are classically described as a “bihilar butterfly”pattern. Typically, these reach a maximum at 24 – 48 hours and resolve slowlyover 7 days in survivors. Progression of infiltrates after 48 hours indicates ARDSor pneumonia.

The slightest respiratory sign or symptom calls for a chestX-ray and observation for six hours, including pulse oximetry.

Figure 19.8

Bilateral “butterfly” pulmonary infiltrates :central consolidation, compatible with lungcontusion is seen in the chest X-ray.

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19.7.3 Assessment of patients with suspected lung injury

Of the three clinical presentations mentioned above, immediate respiratorydistress and ARDS are self-evident. The diagnostic problem lies with the insidiousdevelopment of BLI and, therefore, begs the question of how long to keep patientsunder observation.

The real world scenario of actual time elapsed since exposure to the blast resemblesthe following picture.

1. Casualties of an explosion are transported to the hospital, and reach it withsome delay.

2. Confusion in the emergency reception is common during the triage of masscasualties and results in more time passing by.

3. All dazed but stable patients without clinically significant injury are classedCategory III and sent off to a holding area, with further passage of time.

4. These patients usually have minor wounds and bruises; many have sensorineuraldeafness or even a ruptured eardrum. They still need to be examined properly,which results in further delay. They are often also frightened and require some

calming down before discharge can be considered.By this time, the scenario is well into the first couple of hours after exposure, if notmore. Any patient who does have pulmonary injury, and who did not have symptomsoriginally, will start presenting some symptoms before reaching the point of discharge.Re-examination in the holding area will send this patient into the hospital.

19.7.4 Patient management

Not all patients suffering from BLI require intubation and mechanical ventilation;only severe cases presenting respiratory distress or progressing insufficiency withhypoxaemia do. Treatment of blast lung is challenging even with the aid of mechanicalventilation; high ventilation pressures increase the risk of air embolism or tensionpneumothorax and should be avoided. If mechanical ventilation is available, thesimplest recommended protocol is permissive hypercapnoea, and high-frequency,high-oxygen flow by means of a small naso-gastric tube inserted into the trachea,made easier by a tracheostomy. Tidal volumes should be decreased (5 – 7 ml/kginstead of 8 – 10) and peak airway pressure kept low.

Any pneumo- or haemothorax should be treated immediately; some surgical teamsintroduce bilateral prophylactic chest tubes.

The usual situation when working with limited resources is that intubation withmechanical ventilation is not available and only supportive treatment can be instituted:• supplemental oxygen;

• suctioning of blood and secretions;• tracheostomy in severe cases to facilitate suctioning, which also reduces the effort

of breathing;• meticulous fluid balance to ensure tissue perfusion, while keeping i.v. crystalloids

to a minimum to decrease lung oedema;• control of chest-wall pain if present – i.v. analgesics, intercostal nerve block;• regular change of position, including prone; and• good chest physiotherapy.

Positioning of the patient can be done as a clinical test. The lateral position with theunaffected or less affected side up allows for better ventilation and less bleeding intothe good lung. On the other hand, gravity may augment the blood flow to the lower

injured lung, increasing the bleeding and oedema. The test is performed with thegood side up first: if the condition of the patient is improved, it is maintained. If not,the position is reve

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